APOPTOTIC CELL-DEATH INDUCED BY OPTIC-NERVE LESION IN THE NEONATAL RAT

Citation
Sa. Rabacchi et al., APOPTOTIC CELL-DEATH INDUCED BY OPTIC-NERVE LESION IN THE NEONATAL RAT, The Journal of neuroscience, 14(9), 1994, pp. 5292-5301
Citations number
47
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
02706474
Volume
14
Issue
9
Year of publication
1994
Pages
5292 - 5301
Database
ISI
SICI code
0270-6474(1994)14:9<5292:ACIBOL>2.0.ZU;2-N
Abstract
Cell death can be ascribed to one of two distinct modes of degeneratio n: apoptosis (programmed or active cell death) or necrosis (passive de generation). While apoptosis is generally assumed to occur in physiolo gical conditions such as normal development or tissue turnover, necrot ic cell degeneration is induced in pathological situations. Here we re port that also in a pathological situation, such as after axotomy in t he CNS, apoptotic type of cell death comes into play: following intrac ranial transection of the optic nerve in the neonatal rat in vivo, ret inal ganglion cells undergo an active, apoptotic cell death. In fact, the administration of protein synthesis inhibitors (actinomycin D and cycloheximide) prevents the appearance of pyknotic nuclei as well as o f fragmented DNA of ganglion cells at 24 hr postlesion. Correspondingl y, the number of surviving cells after actinomycin D and cycloheximide treatment is comparable to normal, unlesioned retinas. In addition, c ycloheximide decreases the number of pyknotic ganglion cells during sp ontaneous cell death.